Question

Your team has posed the question: Does MAD1 control the metaphase checkpoint? The hypothesis was: If MAD1 gives the signal to progress to anaphase after chromosomes have aligned, then a group of mutant MAD1 cells will more often have imperfect chromosome numbers after a series of cell divisions compared to normal cells.You investigated this question by comparing the cell division of cells that have the normal, or “wildtype” MAD1 gene to the division of cells with the mutant MAD1 gene. In your experiments, you compared the number of “aneuploid” cells (imperfect chromosome numbers) to the number of “euploid” (correct chromosome numbers) in your experimental group of MAD1 mutant cells and your control group of MAD1 normal cells.

Percent Aneuploid cells in Sample (incorrect chromosome number)
	Sample 1	Sample 2	Sample 3	Sample 4	Average	Standard Deviation
Control: Normal MAD1 cells	7%	15%	8%	13%	10.75%	3.86
Experimental: Mutant MAD1 cells	30%	25%	37%	29%	30.25%	4.99

Results: Average Percent of Aneuploid Cells after 24 hrs

Control:Normal MAD1 cells had an average of 10 percent aneuploid cells after 24 hours.

Experimental: Mutatnt MAD1 cells had an average of 30 percent aneuploid cells after 24 hours

Question:

Develop a conclusion based on these results. Is the hypothesis supported or rejected? Explain your reasoning.

Answer 1

Please find the answers below:

Conclusion: According to the information, it was hypothesized that presence of MAD1 prevents observance of incorrect chromosomes in the cells. Thus, ideally, the wild type cells containing a normal copy of MAD1 must exhibit a normal cellular division while the mutant cells containing improper MAD1 must show incorrect chromosomes. The tabulated data shows that the average number of control or normal cells is very less in this case with a very few standard deviation thus showing that the MAD1 is indeed required normally to allow cellular division to take place. Similarly, the mutant MAD1 cells extremely high average number of faulty chromosomes with extremely low standard deviation. These corroborating observations, thus, validate the essential role of MAD1 in maintaining normal cellular division in cells and distribution of chromosomes in the daughter cells.

Based upon the data and the conclusion, it can be stated that the hypothesis is supported.